In vivo evidence for chylomicrons as mediators of postprandial inflammation

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M.A. de Vries, B. Klop, A. Alipour, G.J.M. van de Geijn, J.W. Janssen, P. Valdivielso, J.R. Villodres, J. Ram’rez Bollero, M. Castro Cabezas

Voorzitter(s): prof. dr. M.M.E. Schneider, UMCU, Utrecht & dr. L.J.M. de Heide, Zorgroep Noorderbreedt, Leeuwarden

Woensdag 22 april 2015

15:00 - 16:00u in Zaal 0.4

Categorieën: parallelsessie (case reports/research)

Parallel sessie: Parallelsessie 3: Case reports/research

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Background:
The postprandial situation is a pro-inflammatory condition linked to the development of atherosclerosis. We evaluated the relationship between apolipoprotein (apo) B48 and postprandial leukocyte activation.

Methods:
Leukocyte activation markers were measured by flow cytometry in patients with and without coronary artery disease (CAD). In 12 healthy subjects, leukocyte activation markers, triglycerides and apo B48 were determined after an oral fat load.

Results:
94 patients were included. Fasting apo B48 was significantly higher in patients with CAD (n=56, 7.9 ± 4.9 mg/L) than in subjects without CAD (n=38, 5.7 ± 3.7 mg/L, p=0.019), and higher in males (n=51, 8.0 ± 4.8 mg/L) than in females (n=43, 5.8 ± 4.0 mg/L, p=0.025). Fasting apo B48 and triglycerides correlated positively with fasting monocyte CD11b and granulocyte CD66b expression. No correlations were found between these inflammatory markers and plasma total apo B or LDL-C. Plasma apo B48 increased after an oral fat load (n=12), with the maximal increase after 2 hours, from 3.6 ± 1.9 mg/L to 6.4 ± 3.1 mg/L (p<0.001). Monocyte CD11b expression also increased, with the maximal increase after 4 hours, from 14.8 ± 2.3 au to 16.5 ± 2.2 au (p=0.043). The postprandial apo B48 response correlated positively with postprandial monocyte CD11b (Spearman’s rho: 0.615, p=0.033), but no correlations were found between postprandial triglycerides and postprandial leukocyte activation markers.

Conclusion:
This study suggests that chylomicrons may be directly responsible for postprandial leukocyte activation. The postprandial chylomicron response may be a stronger mediator of postprandial inflammation than postprandial triglyceridemia.